Abstract
From the beginning of their lives, cancer cells exert a procoagulant activity in their microenvironment, which can extend systemically and become clinically evident as Trousseau's syndrome, the well-known association between tumor and thrombosis. It is becoming clear that the genetic mechanisms responsible for neoplastic transformation (activation of oncogenes such as RAS or MET, and inactivation of tumor suppressor genes such as p53 or PTEN) directly induce the expression of genes controlling hemostasis. Activation of blood coagulation results in a selective advantage for cancer cells, as fibrin provides a scaffold for anchorage and invasion, and coagulation proteins induce receptor-mediated intracellular signals promoting invasive growth. Targeting the tumor procoagulant activity can fight not only a dangerous tumor adverse effect, but also the core mechanisms of cancer onset and progression.
| Original language | English |
|---|---|
| Pages (from-to) | 4827-4833 |
| Number of pages | 7 |
| Journal | Journal of Clinical Oncology |
| Volume | 27 |
| Issue number | 29 |
| DOIs | |
| Publication status | Published - Oct 10 2009 |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
- Medicine(all)
Cite this
Genetic link between cancer and thrombosis. / Boccaccio, Carla; Comoglio, Paolo M.
In: Journal of Clinical Oncology, Vol. 27, No. 29, 10.10.2009, p. 4827-4833.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Genetic link between cancer and thrombosis
AU - Boccaccio, Carla
AU - Comoglio, Paolo M.
PY - 2009/10/10
Y1 - 2009/10/10
N2 - From the beginning of their lives, cancer cells exert a procoagulant activity in their microenvironment, which can extend systemically and become clinically evident as Trousseau's syndrome, the well-known association between tumor and thrombosis. It is becoming clear that the genetic mechanisms responsible for neoplastic transformation (activation of oncogenes such as RAS or MET, and inactivation of tumor suppressor genes such as p53 or PTEN) directly induce the expression of genes controlling hemostasis. Activation of blood coagulation results in a selective advantage for cancer cells, as fibrin provides a scaffold for anchorage and invasion, and coagulation proteins induce receptor-mediated intracellular signals promoting invasive growth. Targeting the tumor procoagulant activity can fight not only a dangerous tumor adverse effect, but also the core mechanisms of cancer onset and progression.
AB - From the beginning of their lives, cancer cells exert a procoagulant activity in their microenvironment, which can extend systemically and become clinically evident as Trousseau's syndrome, the well-known association between tumor and thrombosis. It is becoming clear that the genetic mechanisms responsible for neoplastic transformation (activation of oncogenes such as RAS or MET, and inactivation of tumor suppressor genes such as p53 or PTEN) directly induce the expression of genes controlling hemostasis. Activation of blood coagulation results in a selective advantage for cancer cells, as fibrin provides a scaffold for anchorage and invasion, and coagulation proteins induce receptor-mediated intracellular signals promoting invasive growth. Targeting the tumor procoagulant activity can fight not only a dangerous tumor adverse effect, but also the core mechanisms of cancer onset and progression.
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UR - http://www.scopus.com/inward/citedby.url?scp=70350731332&partnerID=8YFLogxK
U2 - 10.1200/JCO.2009.22.7199
DO - 10.1200/JCO.2009.22.7199
M3 - Article
C2 - 19738115
AN - SCOPUS:70350731332
VL - 27
SP - 4827
EP - 4833
JO - Journal of Clinical Oncology
JF - Journal of Clinical Oncology
SN - 0732-183X
IS - 29
ER -